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NR2F1 controls tumour cell dormancy via SOX9- and RARβ-driven quiescence programmes

Author

Listed:
  • Maria Soledad Sosa

    (Mount Sinai School of Medicine)

  • Falguni Parikh

    (Mount Sinai School of Medicine
    Mount Sinai School of Medicine)

  • Alexandre Gaspar Maia

    (Mount Sinai School of Medicine)

  • Yeriel Estrada

    (Mount Sinai School of Medicine)

  • Almudena Bosch

    (Mount Sinai School of Medicine)

  • Paloma Bragado

    (Mount Sinai School of Medicine)

  • Esther Ekpin

    (Mount Sinai School of Medicine)

  • Ajish George

    (Mount Sinai School of Medicine)

  • Yang Zheng

    (Mount Sinai School of Medicine)

  • Hung-Ming Lam

    (University of Washington)

  • Colm Morrissey

    (University of Washington)

  • Chi-Yeh Chung

    (Mount Sinai School of Medicine)

  • Eduardo F. Farias

    (Mount Sinai School of Medicine
    Tisch Cancer Institute, Mount Sinai School of Medicine)

  • Emily Bernstein

    (Mount Sinai School of Medicine
    Tisch Cancer Institute, Mount Sinai School of Medicine
    Black Family Stem Cell Institute, Mount Sinai School of Medicine)

  • Julio A. Aguirre-Ghiso

    (Mount Sinai School of Medicine
    Mount Sinai School of Medicine
    Tisch Cancer Institute, Mount Sinai School of Medicine
    Black Family Stem Cell Institute, Mount Sinai School of Medicine)

Abstract

Metastases can originate from disseminated tumour cells (DTCs), which may be dormant for years before reactivation. Here we find that the orphan nuclear receptor NR2F1 is epigenetically upregulated in experimental head and neck squamous cell carcinoma (HNSCC) dormancy models and in DTCs from prostate cancer patients carrying dormant disease for 7–18 years. NR2F1-dependent dormancy is recapitulated by a co-treatment with the DNA-demethylating agent 5-Aza-C and retinoic acid across various cancer types. NR2F1-induced quiescence is dependent on SOX9, RARβ and CDK inhibitors. Intriguingly, NR2F1 induces global chromatin repression and the pluripotency gene NANOG, which contributes to dormancy of DTCs in the bone marrow. When NR2F1 is blocked in vivo, growth arrest or survival of dormant DTCs is interrupted in different organs. We conclude that NR2F1 is a critical node in dormancy induction and maintenance by integrating epigenetic programmes of quiescence and survival in DTCs.

Suggested Citation

  • Maria Soledad Sosa & Falguni Parikh & Alexandre Gaspar Maia & Yeriel Estrada & Almudena Bosch & Paloma Bragado & Esther Ekpin & Ajish George & Yang Zheng & Hung-Ming Lam & Colm Morrissey & Chi-Yeh Chu, 2015. "NR2F1 controls tumour cell dormancy via SOX9- and RARβ-driven quiescence programmes," Nature Communications, Nature, vol. 6(1), pages 1-14, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7170
    DOI: 10.1038/ncomms7170
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    Cited by:

    1. Daniela Michelatti & Sven Beyes & Chiara Bernardis & Maria Luce Negri & Leonardo Morelli & Naiara Garcia Bediaga & Vittoria Poli & Luca Fagnocchi & Sara Lago & Sarah D’Annunzio & Nicole Cona & Ilaria , 2024. "Oncogenic enhancers prime quiescent metastatic cells to escape NK immune surveillance by eliciting transcriptional memory," Nature Communications, Nature, vol. 15(1), pages 1-24, December.

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